There are over 250,000 paraplegics in the United States today. Since regeneration of the human spinal cord is abortive, the basic understanding of the potential growth and regenerative capacity of the vertebrate spinal cord is essential for patient management and elimination of this national health problem. The morphological reaction to spinal cord trauma will be studied with light and eletron microscopy to assess the regenerative capacity of this portion of the central nervous system. In addition, the injured spinal cord will be studied to assess some morphological events that increase neuronal receptivity for new synaptic complexes and neuronal growth following injury. The inability of the mammalian injured spinal cord to regenerate axons or axonal sprouts across the site of lesion appears to be, in part, due to the reaction of the neuronal pool in the segment just rostral to the site of hemisection. Folloing spinal cord injury the deafferented motoneurons and interneurons undergo morphological alteration. These neurons are cyclicly reinnervated with different morphological types as well as with varying absolute numbers of presynaptic boutons. The source of these reinnervating presynaptic boutons remains unknown. However, contributions from the major long tracts and spinal interneurons following spinal cord injury are possible. Protein synthetic inhibition results in the growth of centrally derived nerve fibers into the cicatrix. Unfortunately, these nerve fibers degenerate after 30 postoperative days. The mechanism of sustaining this growth pattern during the induced regenerative process will be studied. Lower vertebrate models in which spinal cord regeneration is known to occur will be utilized to assess the ability of these animals to regenerate new neuronal circuits, which result in the return of function, and compare these models of successful regenerative patterns with limited regenerative capacity of the mammalian spinal cord.